In-stent Thrombosis and COVID-19 Infection: Current Insights on the Mechanistic Relationship

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection has been demonstrated as a major risk factor in inducing coronary stent thrombosis due to its propensity to create a pro-thrombotic state. This review explores the mechanisms that may contribute to the increased thrombosis risk seen in COVID-19. Furthermore, we discuss the patient and haematological factors that predispose to an increased risk of stent thrombosis, as well as the role of certain antiplatelet and anticoagulation therapies, including ticagrelor and enoxaparin, that may reduce the likelihood and severity of in-stent thrombosis, in SARS-CoV-2 infection. To counter the pro-inflammatory and pro-thrombotic state shown in COVID-19, anti-thrombotic therapy in the future may be optimised using point-of-care platelet inhibition testing and inflammation-modifying therapies. Large-scale randomised trials with long-term follow-up are increasingly necessary to assess the intersection of COVID-19 and stent optimisation as well as the reduction of stent thrombosis after drug-eluting stent (DES) implantation.

Automated summary

This review examines the increased risk of coronary stent thrombosis in patients with SARS-CoV-2 infection and discusses the mechanisms, patient factors, and treatments that may influence this risk. The use of antiplatelet and anticoagulation therapies, such as ticagrelor and enoxaparin, may help reduce the severity and likelihood of in-stent thrombosis in COVID-19. Future optimization of thrombotic therapy may involve point-of-care platelet inhibition testing and inflammation-modifying therapies. Large-scale randomized trials with long-term follow-up are needed to further explore the intersection of COVID-19 and stent optimization, as well as the reduction of stent thrombosis after drug-eluting stent (DES) implantation.